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Electrolyte & Blood Pressure : E & BP Dec 2022Bartter syndrome (BS) is one of the most well-known hereditary tubular disorders, characterized by hypokalemic, hypochloremic metabolic alkalosis, and... (Review)
Review
Bartter syndrome (BS) is one of the most well-known hereditary tubular disorders, characterized by hypokalemic, hypochloremic metabolic alkalosis, and polyuria/polydipsia. This disease usually presents before or during infancy, and adult nephrologists often inherit the patients from pediatric nephrologists since this is a life-long condition. Here, a few case scenarios will be presented to recount how they first got diagnosed and how their clinical courses were during childhood until adulthood, in addition to a brief review of the disease and its treatment.
PubMed: 36688207
DOI: 10.5049/EBP.2022.20.2.49 -
Frontiers in Endocrinology 2023Copeptin is cleaved from the same precursor as arginine vasopressin and is released in equimolar amounts with arginine vasopressin from the posterior pituitary in... (Review)
Review
Copeptin is cleaved from the same precursor as arginine vasopressin and is released in equimolar amounts with arginine vasopressin from the posterior pituitary in response to the same stimuli. Its level of stability in the blood, quick and simple analysis, and ease of automation make it much easier to analyze than arginine vasopressin, thereby offering a suitable alternative to measuring arginine vasopressin in endocrine disorders. Research has demonstrated the suitability of copeptin in adults for the differentiation of arginine vasopressin resistance and arginine vasopressin deficiency from primary polydipsia, in addition to the early identification of arginine vasopressin deficiency following pituitary surgery; however, further research is still required in the Syndrome of Inappropriate Antidiuretic Hormone (SIADH) and the pediatric population.
Topics: Child; Adult; Humans; Diabetes Insipidus, Neurogenic; Glycopeptides; Arginine Vasopressin; Arginine
PubMed: 37859988
DOI: 10.3389/fendo.2023.1230045 -
Endocrinology, Diabetes & Metabolism... Oct 2021Hyponatraemia is the most common electrolyte disturbance in hospitalised patients and is associated with numerous adverse outcomes. Patients with schizophrenia are...
SUMMARY
Hyponatraemia is the most common electrolyte disturbance in hospitalised patients and is associated with numerous adverse outcomes. Patients with schizophrenia are particularly susceptible to hyponatraemia, in part due to the close association between this condition and primary polydipsia. We report the case of a 57-year-old woman with schizophrenia and primary polydipsia who was receiving inpatient psychiatric care. She became increasingly confused, had multiple episodes of vomiting, and collapsed 1 week after being commenced on quetiapine 300 mg. On examination, she was hypertensive and her Glasgow coma scale was nine. She had a fixed gaze palsy and a rigid, flexed posture. Investigations revealed extreme hyponatraemia with a serum sodium of 97 mmol/L. A CT brain demonstrated diffused cerebral oedema with sulcal and ventricular effacement. A urine sodium and serum osmolality were consistent with SIAD, which was stimulated by the introduction of quetiapine. The antidiuretic effect of vasopressin limited the kidney's ability to excrete free water in response to the patients' excessive water intake, resulting in extreme, dilutional hyponatraemia. The patient was treated with two 100 mL boluses of hypertonic 3% saline but deteriorated further and required intubation. She had a complicated ICU course but went on to make a full neurological recovery. This is one of the lowest sodium levels attributed to primary polydipsia or second-generation antipsychotics reported in the literature.
LEARNING POINTS
The combination of primary polydipsia and SIAD can lead to a life-threatening, extreme hyponatraemia. SIAD is an uncommon side effect of second-generation anti-psychotics. Serum sodium should be monitored in patients with primary polydipsia when commencing or adjusting psychotropic medications. Symptomatic hyponatraemia is a medical emergency that requires treatment with boluses of hypertonic 3% saline. A serum sodium of less than 105 mmol/L is associated with an increased risk of osmotic demyelination syndrome, therefore the correction should not exceed 8 mmol/L over 24 h.
PubMed: 34653996
DOI: 10.1530/EDM-21-0028 -
Indian Journal of Endocrinology and... 2016Diabetes insipidus (DI) is a hereditary or acquired condition which disrupts normal life of persons with the condition; disruption is due to increased thirst and passing... (Review)
Review
Diabetes insipidus (DI) is a hereditary or acquired condition which disrupts normal life of persons with the condition; disruption is due to increased thirst and passing of large volumes of urine, even at night. A systematic search of literature for DI was carried out using the PubMed database for the purpose of this review. Central DI due to impaired secretion of arginine vasopressin (AVP) could result from traumatic brain injury, surgery, or tumors whereas nephrogenic DI due to failure of the kidney to respond to AVP is usually inherited. The earliest treatment was posterior pituitary extracts containing vasopressin and oxytocin. The synthetic analog of vasopressin, desmopressin has several benefits over vasopressin. Desmopressin was initially available as intranasal preparation, but now the oral tablet and melt formulations have gained significance, with benefits such as ease of administration and stability at room temperature. Other molecules used for treatment include chlorpropamide, carbamazepine, thiazide diuretics, indapamide, clofibrate, indomethacin, and amiloride. However, desmopressin remains the most widely used drug for the treatment of DI. This review covers the physiology of water balance, causes of DI and various treatment modalities available, with a special focus on desmopressin.
PubMed: 26904464
DOI: 10.4103/2230-8210.172273 -
Swiss Medical Weekly 2017Primary polydipsia (PP) has been defined as excessive intake of fluids. However, the pathogenesis of PP remains unexplored. Different theories include a dysfunction in... (Review)
Review
Primary polydipsia (PP) has been defined as excessive intake of fluids. However, the pathogenesis of PP remains unexplored. Different theories include a dysfunction in the thirst mechanism, involvement of the hippocampus, stress-reducing behaviour and lesion occurrences in specific areas of the brain. Most studies have been performed in the psychiatric setting, indicating that PP coincides with schizophrenia, anxiety disorder and depression. However, an increasing number of case reports emphasise the incidence of PP in non-psychiatric patients. As often recommended by healthcare professions and in life-style programmes, the phenomenon of excessive fluid intake appears to be growing, especially in health-conscious and active people. PP is part of the polyuria-polydipsia syndrome, so the differential diagnosis diabetes insipidus (central or nephrogenic) must be excluded. The gold standard when differentiating between these disorders has been the water deprivation test. However, new options for distinguishing between these entities have been proposed e.g., measurement of copeptin, a reliable surrogate marker of the hormone arginine vasopressin (AVP). The major risk of excessive drinking is the development of hyponatraemia and the ensuing complications. In patients with PP, factors reducing the renal excretory capacity of the kidney such as acute illness, medications or low solute intake may accumulate in hyponatraemia. Treatment options for PP remain scarce. Different medication and behavioural therapy have been investigated, but never on a large scale and rarely in non-psychiatric patients. This review provides an overview of the pathophysiology, characteristics, complications, and outcomes of patients with PP in the medical and psychiatric patient.
Topics: Arginine Vasopressin; Diabetes Insipidus; Diagnosis, Differential; Humans; Hyponatremia; Polydipsia, Psychogenic; Schizophrenia
PubMed: 29120013
DOI: 10.4414/smw.2017.14514 -
World Journal of Diabetes May 2023An efficient coronavirus disease 2019 (COVID-19) vaccine is urgently required to fight the pandemic due to its high transmission rate and quick dissemination. There have... (Review)
Review
An efficient coronavirus disease 2019 (COVID-19) vaccine is urgently required to fight the pandemic due to its high transmission rate and quick dissemination. There have been numerous reports on the side effects of the COVID-19 immu-nization, with a focus on its negative effects. Clinical endocrinology is extremely interested in the endocrine issue that arises after receiving the COVID-19 vaccine. As was already mentioned, after receiving the COVID-19 vaccine, many clinical problems could occur. Additionally, there are some compelling reports on diabetes. After receiving the COVID-19 vaccine, a patient experienced hyperosmolar hyperglycemia state, a case of newly-onset type 2 diabetes. There has also been information on a potential connection between the COVID-19 vaccine and diabetic ketoacidosis. Common symptoms include thirst, polydipsia, polyuria, palpitations, a lack of appetite, and weariness. In extremely rare clinical circumstances, a COVID-19 vaccine recipient may develop diabetes complications such as hyperglycemia and ketoacidosis. In these circumstances, routine clinical care has a successful track record. It is advised to give vaccine recipients who are vulnerable to problems, such as those with type 1 diabetes as an underlying illness, extra attention.
PubMed: 37273244
DOI: 10.4239/wjd.v14.i5.560 -
The Pan African Medical Journal 2018
Review
Topics: Adult; Erdheim-Chester Disease; Female; Humans; Immunologic Factors; Interferon-alpha; Polydipsia; Polyuria; Treatment Outcome
PubMed: 29875943
DOI: 10.11604/pamj.2018.29.62.4088 -
Indian Journal of Psychiatry Apr 2011To the best of our knowledge psychogenic polydipsia has not been reported in an Indian journal. We are reporting one such case, which was diagnosed as having depression...
To the best of our knowledge psychogenic polydipsia has not been reported in an Indian journal. We are reporting one such case, which was diagnosed as having depression according to ICD 10 R criteria. Fully investigated patient had some reversible changes in the urinary tract. There was no antidiuretic hormone-related abnormality as indicated by absence of hyponatremia. The patient recovered with antidepressant drugs. The followup was done for 6 months.
PubMed: 21772654
DOI: 10.4103/0019-5545.82554 -
BMJ Case Reports Jul 2014A 13-year-old boy presented with fever, skeletal pain, polydipsia, polyuria and multiple osteolytic lesions in pelvic bones and upper femur. There was no organomegaly or...
A 13-year-old boy presented with fever, skeletal pain, polydipsia, polyuria and multiple osteolytic lesions in pelvic bones and upper femur. There was no organomegaly or lymphadenopathy. His serum calcium levels were raised. Peripheral blood film examination was normal. Bone marrow showed presence of blast cells. Flowcytometry indicated B-acute lymphoblastic leukaemia (B-ALL). Hypercalcaemia and osteolytic lesions are rare presentations of B-ALL. This should be kept as a differential if a child presents with unexplained skeletal pain with lytic lesions.
Topics: Adolescent; Bone Marrow; Bone Marrow Examination; Bone and Bones; Humans; Hypercalcemia; Male; Musculoskeletal Pain; Osteolysis; Polydipsia; Polyuria; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma; Radiography
PubMed: 25006054
DOI: 10.1136/bcr-2014-204050 -
Schizophrenia Research Aug 2014To identify the mechanism of unexplained hyponatremia and primary polydipsia in schizophrenia and its relationship to the underlying psychiatric illness. (Review)
Review
OBJECTIVE
To identify the mechanism of unexplained hyponatremia and primary polydipsia in schizophrenia and its relationship to the underlying psychiatric illness.
METHODS
Briefly review previous studies that led to the conclusion the hyponatremia reflects altered hippocampal inhibition of peripheral neuroendocrine secretion. In greater detail, present the evidence supporting the hypothesis that circuit dysfunction associated with the hyponatremia and the polydipsia contributes to the underlying mental disorder.
RESULTS
Polydipsic patients with and without hyponatremia exhibit enhanced neuroendocrine responses to psychological stress in proportion to structural deformations on their anterior hippocampus, amygdala and anterior hypothalamus. Nonpolydipsic patients exhibit blunted responses and deformations on other hippocampal and amygdala surfaces. The deformations in polydipsic patients are also proportional to diminished peripheral oxytocin levels and impaired facial affect recognition that is reversed by intranasal oxytocin. The anterior hippocampus is at the hub of a circuit that modulates neuroendocrine and other responses to psychological stress and is implicated in schizophrenia. Preliminary data indicate that other measures of stress reactivity are also enhanced in polydipsics and that the functional connectivity of the hippocampus with the other structures in this circuitry differs in schizophrenia patients with and without polydipsia.
CONCLUSION
Polydipsia may identify a subset of schizophrenia patients whose enhanced stress reactivity contributes to their mental illness. Stress reactivity may be a symptom dimension of chronic psychosis that arises from circuit dysfunction that can be modeled in animals. Hence polydipsia could be a biomarker that helps to clarify the pathophysiology and heterogeneity of psychosis as well as identify novel therapies. Clinical investigators should consider obtaining indices of water balance, as these may help them unravel and more concisely interpret their findings. Basic researchers should assess if the polydipsic subset is a patient group particularly suitable to test hypotheses arising from their translational studies.
Topics: Animals; Brain; Chronic Disease; Humans; Hyponatremia; Neural Pathways; Polydipsia; Schizophrenia; Stress, Psychological
PubMed: 24994556
DOI: 10.1016/j.schres.2014.06.001